Earlier workers have demonstrated that the muscle of the mitral valve contracts in vitro, possess both adrenergic and cholinergic nerves, and demonstrates intracellular action potentials. In previous work, we have shown that the valve muscle is electrically and mechanically active in situ. The proposed experiments are designed to establish the role of this muscular structure in normal cardiac function. We hope to determine: 1. whether contraction of the leaflet muscle opposes the bulging of the valve leaflets into the atrium during ventricular systole; 2. whether the contractility of the valve musculature can be modulated by the cardiac nerves; and 3. the effects of cardiac arrhythmias. Leaflet displacement (LD), atrioventricular pressures, and the ECG will be recorded from dogs on cardiopulmonary bypass. The relationship of LD to the ventriculoatrial pressure gradient (delta-V-A) will be determined under control conditions and after destruction of the leaflet muscle with phenol. In other experiments, LD will be examined in response to both sympathetic and parasympathetic nerve stimulation. The relationship of LD to delta-V-A will be determined in the presence and absence of stimulation, before and after valve denervation, to determine whether it is affected by automomic neural activity. Finally, LD will be studied both on and off cardiac bypass to determine the effect of artificially-induced cardiac arrhythmias on leaflet contraction and LD, respectively. We hope to discover whether the A-V valves are only passive flaps of tissue which respond to transvalvular pressure gradients or whether active contraction of the valve muscle plays an important role in valve closure and the prevention of excessive atrial bulging of the leaflets during ventricular systole. Such information may be very useful in explaining valvular malfunction which occurs in the absence of any demonstrable valvular disease process.